To test the hypothesis that there is excessive renal glucose production in people with type 2 diabetes mellitus and to test the hypothesis that insulin suppresses RGP in normal humans and that this suppression is impaired in NIDDM. To test the hypothesis that the human kidney contributes to the to the compensatory increase in appearance of glucose in plasma during hypoglycmia and this is impared in NIDDM; is an important site of postprandial uptake of glucose and release of lactate and alanine.